Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P392

ECE2007 Poster Presentations (1) (659 abstracts)

Less-calcemic vitamin D analogs enhance biological responses and modulate responsiveness to gonadal steroids in skeletal tissues

Dalia Somjen 1 , Gary H Posner 2 , Yosef Weisman 1 & Alvin M Kaye 3

1Tel- Aviv Sourasky Medical Center, Tel-Aviv, Israel; 2The Johns Hopkins University, Baltimore, MD., United States; 3The Weizmann Institute of Science, Rehovot, Israel.

Vitamin D metabolites modulate creatine kinase specific activity (CK) in cultured skeletal cells. In this study we assess the effect of vitamin D metabolites on CK in rat epiphyseal cartilage (Ep) and diaphyseal bone (Di). Female or male Wistar- derived rats were used either as intact or after gonadectomy (Ovx or cast respectively), and treatments started 2 weeks post surgery. Rats were injected daily for 1, 2 or 8 weeks with the less-calcemic vitamin D analogs CB 1093 (CB), JKF 1624F2-2 (JKF) or QW 1624F2-2 (QW) and 24hrs after the last analog injection, rats were injected with E2, raloxifene (Ral) or tamoxifen (TAM) or both in females or dihydrotestosterone (DHT) in males, and organs were collected for CK measurements and western blot analysis for estradiol receptor ( (ERα) 24hrs after last injection. CK was lower in Ep and Di from vitamin D- depleted than in vitamin D- replete rats. Moreover E2 or DHT, which increases CK in Ep and Di of intact female or male rats, stimulated CK to a much lower extent in vitamin D- depleted rats. Treatment of intact female rats for 2 or 8 weeks with JKF or QW, upregulated the E2 – or DHT- response of CK in Ep and Di, without affecting constituent levels. All vitamin D analogs enhanced the CK response to Ral and TAM in these organs, but the inhibitory effect of Ral or TAM on E2-induced CK was lost. CB induced also ER( protein in Ep and Di from intact and Ovx female rats. In conclusion, vitamin D induces CK and upregulates the response and sensitivity of CK to E2 and SERMs, possibly via increased ER( protein. These results corroborate our in vitro studies in human bone cells and provide evidence that vitamin D is crucial to maintain normal skeletal energy metabolism.

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